Review articleThe central nervous system – An additional consideration in ‘rotator cuff tendinopathy’ and a potential basis for understanding response to loaded therapeutic exercise
Introduction
Tendinopathy is a term commonly used to describe tendon pathology and/or pain. Despite being a well-recognised clinical presentation, a definitive understanding of the pathoaetiology of rotator cuff tendinopathy remains elusive (Lewis, 2009). Over recent years there has been a focus upon understanding pain associated with tendinopathy from the perspective of local tissue based pathology. But, in light of the well-recognised dissociation between pathology and pain (Cook and Purdam, 2009, Drew et al., 2012), it is becoming clear that additional explanatory models are now needed (Drew et al., 2012).
In view of this, the aim of this paper is to present a theoretical extension to current models incorporating the integral role of the central nervous system (CNS) in the pain experience. For the purpose of clarity within this paper and to aid clinical translation, the terminology ‘rotator cuff tendinopathy’ refers to a presentation where a person complains of shoulder pain with movement that is provoked further with load, for example lifting or through resisted tests performed by a clinician during a physical examination (Littlewood et al., 2012a).
We recognise that the reader might object to or question the appropriateness of the term rotator cuff tendinopathy for two reasons. Firstly, the criteria we use to define rotator cuff tendinopathy is broad and might include a range of biomedical diagnoses, including subacromial impingement, subacromial bursitis, rotator cuff tear, acromioclavicular joint osteoarthritis etc. However, in the absence of evidence to support the validity or reliability of such diagnoses (May et al., 2010), particularly in relation to the lack of association between pathology and pain, it is difficult to substantiate such an objection. Secondly, in the context of attempts to highlight the role of the CNS, such specific pathology or impairment terminology might be regarded as a backwards step because of their reference to specific peripheral tissue or mechanical mechanisms. However, such a broad definition of tendinopathy in this translational paper is deliberate and purposeful to highlight how current practice models can be interpreted and usefully enhanced without wholesale, probably unrealistic, changes to practice and terminology; hence there is pragmatic value.
A secondary aim is to offer a potential rationale to explain the favourable response to loaded therapeutic exercises demonstrated by previous studies (Jonsson et al., 2005, Bernhardsson et al., 2010, Holmgren et al., 2012, Littlewood et al., 2012a). These further considerations have the potential to offer a useful basis upon which to explain pain to patients and for clinicians to prescribe appropriate therapeutic management strategies.
Section snippets
Local tissue pathology-pain models
This paper will begin by offering a critique of local pain models as a basis upon which to justify the need for greater consideration of the CNS. Tissue based pathology-pain models have been proposed (Cook and Purdam, 2009) and adapted to the rotator cuff (Lewis, 2010). However, as mentioned, these models are confounded by the lack of association between pathology and pain (Cook and Purdam, 2009, Drew et al., 2012). Using magnetic resonance imaging, Frost et al. (1999) could not distinguish
Local biochemical models
In light of the shortcomings of local tissue pathology-pain models, others have suggested a local biochemical basis for the pain associated with tendinopathy where biochemical mediators in the tissue stimulate nocioceptive afferent fibres (Khan et al., 2000). Degenerative pathology is associated with neurovascular ingrowth and potential pain mediators such as substance P and acetylcholine. However, it remains unclear whether biochemical substances are a cause of tissue degradation and/or pain
Background to the role of the CNS
A contemporary understanding of pain suggests that there might be other mechanisms involved in pain associated with tendinopathy that might act with the local mechanisms outlined above or in isolation. The notion that the state of the tissue does not provide an adequate measure of pain is recognised in relation to other pain syndromes (Moseley, 2007, Melzack and Wall, 2008) but in tendinopathy local tissue/biochemical based models are predominantly used to explain pain (Cook and Purdam, 2009,
Explaining pain
The following section describes the potential mechanisms involved in pain associated with rotator cuff tendinopathy. The aim is to offer a reasoned explanation as to why pain state or output might persist and might not be proportionate to the state of the rotator cuff tissue. In addition to enhancing understanding of pain mechanisms, one further consequence of this might be a direct challenge to current practice where, for example, prescription of loaded exercise is limited due to fear of
Rationale for response to loaded therapeutic exercise
From a biological perspective initially, tendons are regarded as being mechanosensitive, which means they are capable of responding to mechanical stimuli (Maffulli and Longo, 2008). The term ‘mechanotherapy’ has been coined to describe how a programme of structured exercise might stimulate human tissue and reverse tendon de-conditioning (Reeves, 2006, Abate et al., 2009, Khan and Scott, 2011). It is proposed that a progressive exercise regime will stimulate a process of re-conditioning and
Conclusion
The cause of pain associated with rotator cuff tendinopathy remains uncertain and there are clear limitations associated with current explanatory models that rely on a peripheral tissue based understanding. A theoretical addition to these pre-existing models has been presented with reference to current literature incorporating the integral role of the CNS in any pain experience. This additional consideration offers an accessible way to understand the pain associated with rotator cuff
Acknowledgement
This work was produced by Chris Littlewood under the terms of a Doctoral Research Fellowship issued by the Secretary of State for Health. The funding body have played no role in the design, writing of the protocol manuscript or decision to submit for publication.
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